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Fig. 3 | Experimental Hematology & Oncology

Fig. 3

From: Roles of N6-methyladenosine (m6A) modifications in gynecologic cancers: mechanisms and therapeutic targeting

Fig. 3

In EC, m6A regulatory proteins contribute to tumorigenesis and metastasis by interacting with various RNAs. METTL14 mutation or reduced expression of METTL3 increases the proliferation and tumorigenicity of EC by activating the AKT pathway. WTAP downregulates CAV‐1 expression to activate the NF‐κB signaling pathway in EC, promoting EC progression. HIF-1α and HIF-2α activate the expression of ALKBH5 under hypoxic conditions, facilitating the SOX2 expression by demethylating the SOX2 mRNA, leading to the tumorigenesis of EC. ALKBH5 demethylates the target transcript IGF1R and enhances its mRNA stability to promote tumorigenesis and metastasis of EC. FTO promotes HOXB13 protein expression, activates the WNT signaling pathway, and promotes EC invasion and metastasis. PADI2 activates the IGF2BP1 expression and helps in maintaining the mRNA stability and expression of SOX2, thereby supporting the malignancy state of EC. IGF2BP1 recruits PABPC1 to promote PEG10 protein expression, contributing to the tumorigenesis of EC. YTHDF2 inhibits the expression of IRS1 and inhibits IRS1/AKT signaling pathway, consequently inhibiting the tumorigenicity of EC. YTHDF2-mediated LncRNA FENDRR degradation promotes cellular proliferation by elevating the SOX4 expression in EC

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